Mossialos D, Meyer J M, Budzikiewicz H, Wolff U, Koedam N, Baysse C, Anjaiah V, Cornelis P
Department of Immunology, Parasitology, and Ultrastructure, Flanders Interuniversity Institute for Biotechnology, Belgium.
Appl Environ Microbiol. 2000 Feb;66(2):487-92. doi: 10.1128/AEM.66.2.487-492.2000.
Transposon mutant strain 3G6 of Pseudomonas fluorescens ATCC 17400 which was deficient in pyoverdine production, was found to produce another iron-chelating molecule; this molecule was identified as 8-hydroxy-4-methoxy-quinaldic acid (designated quinolobactin). The pyoverdine-deficient mutant produced a supplementary 75-kDa iron-repressed outer membrane protein (IROMP) in addition to the 85-kDa IROMP present in the wild type. The mutant was also characterized by substantially increased uptake of (59)Fe-quinolobactin. The 75-kDa IROMP was produced by the wild type after induction by quinolobactin-containing culture supernatants obtained from the pyoverdine-negative mutant or by purified quinolobactin. Conversely, adding purified wild-type pyoverdine to the growth medium resulted in suppression of the 75-kDa IROMP in the pyoverdine-deficient mutant; however, suppression was not observed when Pseudomonas aeruginosa PAO1 pyoverdine, a siderophore utilized by strain 3G6, was added to the culture. Therefore, we assume that the quinolobactin receptor is the 75-kDa IROMP and that the quinolobactin-mediated iron uptake system is repressed by the cognate pyoverdine.
荧光假单胞菌ATCC 17400的转座子突变株3G6缺乏绿脓菌素的产生，但发现它能产生另一种铁螯合分子；该分子被鉴定为8-羟基-4-甲氧基喹哪啶酸（命名为喹诺菌素）。除了野生型中存在的85 kDa铁调节外膜蛋白（IROMP）外，缺乏绿脓菌素的突变体还产生了一种补充性的75 kDa IROMP。该突变体的另一个特征是对（59）Fe-喹诺菌素的摄取大幅增加。野生型在由缺乏绿脓菌素的突变体获得的含喹诺菌素的培养上清液或纯化的喹诺菌素诱导后产生75 kDa IROMP。相反，向生长培养基中添加纯化的野生型绿脓菌素会导致缺乏绿脓菌素的突变体中75 kDa IROMP受到抑制；然而，当添加3G6菌株利用的铁载体铜绿假单胞菌PAO1绿脓菌素到培养物中时，未观察到抑制现象。因此，我们假设喹诺菌素受体是75 kDa IROMP，并且喹诺菌素介导的铁摄取系统受到同源绿脓菌素的抑制。
